Drug-induced cholestasis risk assessment in sandwich-cultured human hepatocytes.

Toxicol In Vitro

KaLy-Cell, 20A rue du Général Leclerc, 67115 Plobsheim, France; Université de Franche-Comté, EA4267, 25030 Besançon, France. Electronic address:

Published: August 2016

AI Article Synopsis

  • Drug-induced cholestasis (DIC) is a major cause of drug-induced liver injury (DILI), making early detection of drugs with cholestatic potential important.
  • Researchers developed and validated an in vitro model to assess DIC using human hepatocytes and evaluated the cholestatic potential of 14 training compounds through a drug-induced cholestasis index (DICI).
  • Four compounds (nefazodone, bosentan, perhexiline, troglitazone) were identified as having cholestatic risk, while others were deemed safe, showcasing the model’s usefulness in identifying drugs that may cause liver issues early in the development process.

Article Abstract

Drug-induced cholestasis (DIC) is recognized as one of the prime mechanisms for DILI. Hence, earlier detection of drug candidates with cholestatic signature is crucial. Recently, we introduced an in vitro model for DIC and evaluated its performance with several cholestatic drugs. We presently expand on the validation of this model by 14 training compounds (TCs) of the EU-EFPIA IMI project MIP-DILI. Several batches of human hepatocytes in sandwich-culture were qualified for DIC assessment by verifying the bile acid-dependent increase in sensitivity to the toxic effects of cyclosporin A. The cholestatic potential of the TCs was expressed by determining the drug-induced cholestasis index (DICI). A safety margin (SM) was calculated as the ratio of the lowest TC concentration with a DICI≤0.80 to the Cmax,total. Nefazodone, bosentan, perhexiline and troglitazone were flagged for cholestasis (SM<30). The hepatotoxic (but non-cholestatic) compounds, amiodarone, diclofenac, fialuridine and ximelagatran, and all non-hepatotoxic compounds were cleared as "safe" for DIC. Tolcapone and paracetamol yielded DICI-based SM values equal to or higher than those based on cytotoxicity, thus excluding DIC as a DILI mechanism. This hepatocyte-based in vitro assay provides a unique tool for early and reliable identification of drug candidates with cholestasis risk.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.tiv.2016.03.008DOI Listing

Publication Analysis

Top Keywords

drug-induced cholestasis
12
human hepatocytes
8
cholestasis risk
4
risk assessment
4
assessment sandwich-cultured
4
sandwich-cultured human
4
hepatocytes drug-induced
4
cholestasis dic
4
dic recognized
4
recognized prime
4

Similar Publications

Studying the intracellular bile acid concentration and toxicity in drug-induced cholestasis: Comprehensive LC-MS/MS analysis with human liver slices.

Toxicol In Vitro

January 2025

University of Groningen, Groningen Research Institute of Pharmacy, Department of Pharmaceutical Technology and Biopharmacy, Antonius Deusinglaan 1, 9713 AV Groningen, the Netherlands. Electronic address:

Drug-induced cholestasis (DIC) is a leading cause of drug-induced liver injury post-drug marketing, characterized by bile flow obstruction and toxic bile constituent accumulation within hepatocytes. This study investigates the toxicity associated with intracellular bile acid (BA) accumulation during DIC development. Using liquid chromatography with tandem mass spectrometry (LC-MS/MS) analysis, we examined intracellular BA concentrations in human precision-cut liver slices (PCLS) following the administration of cyclosporin A and chlorpromazine, both with and without an established BA mixture.

View Article and Find Full Text PDF

Vanishing bile duct syndrome (VBDS) is a serious drug induced liver injury characterized by chronic cholestasis and loss of intrahepatic bile ducts. VBDS has been reported also following checkpoint inhibitor treatment. We compared CD3 + , CD4 + , CD8 + , CD20 + , CD57 + , PD-1 + and PD-L1 + lymphocyte infiltrates in liver biopsies of patients that encountered VBDS (n = 2) or hepatotoxicity (n = 3) after pembrolizumab (n = 4) or nivolumab (n = 1) treatment with samples from normal liver (n = 10), non-alcohol steatohepatitis (NASH, n = 10), primary biliary cholangitis (PBC, n = 10) or pembrolizumab-treated patients without adverse events (n = 2).

View Article and Find Full Text PDF

Background And Aims: Short courses of intravenous (iv) methylprednisolone (MP) can cause drug induced liver injury (DILI). The aim of this study was to assess the clinical features and HLA associations of MP-related DILI enrolled in the US DILI Network (DILIN).

Methods: DILIN cases with MP as a suspected drug were reviewed.

View Article and Find Full Text PDF

Obeticholic acid aggravates liver fibrosis by activating hepatic farnesoid X receptor-induced apoptosis in cholestatic mice.

Chem Biol Interact

January 2025

New Drug Screening and Pharmacodynamics Evaluation Center, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China. Electronic address:

Obeticholic acid (OCA) was approved for the treatment of primary biliary cholangitis (PBC) patients. However, it can cause severe drug-induced liver injury (DILI), which may put PBC patients at risk of acute-on-chronic liver failure (ACLF) and even death. Farnesoid X receptor (FXR) is considered as the target of OCA for cholestasis, but there is still a lack of research on whether hepatic and ileal FXR have different effects after OCA treatment.

View Article and Find Full Text PDF

Itch, also known as pruritus, is one of the most prevalent symptoms observed in dermatological practices. Itch frequently arises from primary pruritic dermatoses, although it may also manifest in the absence of a primary pruritic skin rash. The latter itchy condition is referred to as "cutaneous pruritus" in the Japanese guidelines published in 2020.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!